Myocardial injury in a 41-year-old male treated with methylphenidate: a case report.

Background: Elevated cardiac troponin levels are consistent with the diagnosis of an acute coronary syndrome, but may also represent adverse drug reactions. Psychostimulating drugs raise both blood pressure and heart rate, and case reports of sudden death, stroke, and myocardial infarction have led to regulatory and public concern about the cardiovascular safety of these drugs.

Case Presentation: We present a case where a 41-year-old Norwegian male with radiating chest pain, elevated troponins, and supraventricular tachycardia was hospitalized.

Diazoxide protects against doxorubicin-induced cardiotoxicity in the rat.

Aim: Chemotherapy with doxorubicin is limited by cardiotoxicity. Free radical generation and mitochondrial dysfunction are thought to contribute to doxorubicin-induced cardiac failure. In this study we wanted to investigate if opening of mitochondrial KATP-channels by diazoxide is protective against doxorubicin cardiotoxicity, and if 5-hydroxydecanoate (5-HD), a selective mitochondrial KATP-channel antagonist, abolished any protection by this intervention.

Morphine enhances doxorubicin-induced cardiotoxicity in the rat.

Interventions to reduce the cardiotoxicity of doxorubicin are clinically relevant. Pharmacological preconditioning mimicking ischemic preconditioning has been demonstrated with morphine and represents an acceptable clinical intervention. The purpose of this study was to examine if pretreatment in vivo with morphine could reduce doxorubicin-induced cardiotoxicity ex vivo in a rat model.

A short-time model to study relevant indices of cardiotoxicity of doxorubicin in the rat.

Aim: Short-time models (STM) to study the cardiotoxicity (acute or chronic) of doxorubicin in rats are of interest to assess protective interventions and pathways. STM promotes more ethical animal treatment with less stress, and at a lower cost compared to established long-time models (LTM). We wanted to investigate if an STM of 9 d yields the same information regarding cardiotoxicity as an LTM of 9 weeks.